Document Detail

HIP-55/DBNL-dependent regulation of adrenergic receptor mediates the ERK1/2 proliferative pathway.
MedLine Citation:
PMID:  24802081     Owner:  NLM     Status:  Publisher    
The activation of β-adrenergic receptors (β-ARs) plays a key role in regulating cardiac function. However, the detailed regulatory mechanisms of β-AR-induced fibrosis are still unclear. We used a proteomics approach to analyze the changes in protein expression patterns in cardiac fibrosis with β-AR stimulation. HIP-55 (also called debrin-like; DBNL) was revealed as a novel regulator in the signaling regulatory network with β-AR activation. Further studies of both HIP-55-overexpressed and -deficient cardiac fibroblasts indicated that HIP-55 negatively regulated β-AR-activated cardiac fibroblast proliferation and the proliferative signaling pathway may be associated with the extracellular signal-regulated protein kinase (ERK) activation. Our data provide a new mechanistic insight into the role of HIP-55 in β-AR-induced cardiac fibroblast proliferation and suggest a new treatment strategy for proliferative disorders.
Ning Liu; Rui Xing; Chengzhi Yang; Aiju Tian; Zhizhen Lv; Ningning Sun; Xiang Gao; Youyi Zhang; Zijian Li
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-5-7
Journal Detail:
Title:  Molecular bioSystems     Volume:  -     ISSN:  1742-2051     ISO Abbreviation:  Mol Biosyst     Publication Date:  2014 May 
Date Detail:
Created Date:  2014-5-7     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101251620     Medline TA:  Mol Biosyst     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Ionic liquid and deep eutectic solvent-activated CelA2 variants generated by directed evolution.
Next Document:  Fatty Acid Binding Protein 4 Deficiency Protects against Oxygen-Induced Retinopathy in Mice.